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1 Physiologisches Institut und 2 Zentrum für Innere Medizin, Abteilung für Kardiologie, Justus-Liebig-Universität, D-35392 Giessen, Germany
We investigated the relationship between the
ATP-evoked rise of cytosolic Ca2+
concentration
([Ca2+]i)
and barrier function in porcine aortic endothelial monolayers. ATP
(0.01-100 µM) induced a transient rise of
[Ca2+]i
and reduced permeability in a concentration-dependent manner. In
contrast, the Ca2+ ionophore
ionomycin (1 µM) elicited a rise in
[Ca2+]i
comparable to that induced by ATP (10 µM), but it increased permeability. For the reduction of permeability, nucleotides were found
to be in the following order of potency: ATP = ATP
S > ADP = UTP.
Blockade of adenosine receptors by 8-phenyltheophylline (10 µM) did
not affect ATP (10 µM)-induced reduction of permeability. ATP reduced
permeability even in endothelial monolayers that had been loaded with
the Ca2+ chelator BAPTA to prevent
the rise in
[Ca2+]i.
U-73122 (1 µM), an inhibitor of phospholipase C (PLC), completely abolished the effect of ATP (10 µM) on permeability. It also
abolished the translocation of protein kinase C (PKC) in response to
ATP, which could also be achieved by the PKC inhibitors Gö-6976
(100 nM) or bisindolylmaleimide I (1 µM). In the presence of PKC
inhibitors, however, the permeability effect of ATP was not affected.
The presence of inhibitors of adenylate or guanylate cyclase (50 µM SQ-22536 or 20 µM ODQ) prevented changes in cyclic nucleotides but
did not affect the permeability effects of ATP. The study shows that
ATP reduces macromolecule permeability via a PLC-mediated mechanism
that is independent of the concomitant effects of ATP on cytosolic
Ca2+, cyclic nucleotides, or PKC.
adenosine 5'-triphosphate; paracellular permeability; phospholipase C; protein kinase C; cyclic nucleotides
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